The importance of the kidneys in the pathogenesis of arterial hypertension has been widely recognized since the demonstration by Goldblatt and his co-workers1 that lasting hypertension can be produced experimentally by partial constriction of one main renal artery. Page has obtained similar hypertension by compression of the renal parenchyma in the scar of cellophane or silk perinephritis.2 Although several cases of hypertension in human beings have been described in which the condition arose as the apparent result of partial obstruction of renal circulation or as the result of perinephritis, neither abnormality of the large renal vessels nor diffuse perinephritis is commonly present. Lesions of the small renal arterioles, however, are evident even in the early stages of the disease.3 It has therefore been suggested that hypertension may ordinarily arise as the result of spasm and sclerosis of the renal arterioles, functional equivalents of the application of myriads
CORCORAN AC, PAGE IH. RENAL BLOOD FLOW AND SYMPATHECTOMY IN HYPERTENSION. Arch Surg. 1941;42(6):1072–1082. doi:https://doi.org/10.1001/archsurg.1941.01210120107013
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